nonenzymatically interacts and
detoxifies reactive electrophiles and free radicals. NAC was
shown to effectively protect human bronchial fibroblasts against
the toxic effects of tobacco smoke condensates and the isolated
perfused lung against the glutathione (GSH)-depleting effect of
tobacco smoke. NAC was also shown to reduce the reactive oxygen
intermediate hydrogen peroxide (H2O2) and protect against the
toxic effects of H2O2. In vivo studies, however, demonstrated
that NAC when administered orally has very low bioavailability
due to rapid metabolism to GSH among other metabolites. Thus,
even though NAC is very effective in protecting cells of
different origins from the toxicity of reactive components in
tobacco smoke and reactive oxygen species, a direct scavenging
effect by NAC in vivo, particularly when administered orally,
does not seem likely. The bioavailability of NAC itself is very
low when given this route. A more relevant mechanism in vivo for
any protective effect NAC may exert against toxic species may be
due to NAC acting as a precursor of GSH and facilitating its
biosynthesis. GSH will then serve as the protective agent and
detoxify reactive species both enzymatically and
nonenzymatically.